Bernabeu, J., Botella, F. J., & Nebot, M. (2014). Novel T-Violation observable open to any pair of decay channels at meson factories. Phys. Lett. B, 728, 95–98.
Abstract: Quantum entanglement between the two neutral mesons produced in meson factories has allowed the first indisputable direct observation of Time Reversal Violation in the time evolution of the neutral meson between the two decays. The exceptional meson transitions are directly connected to semileptonic and CP eigenstate decay channels. The possibility of extending the observable asymmetries to more decay channels confronts the problem of the “orthogonality condition”, which can be stated with this tonguetwister: Given a decay channel f, which is the decay channel f' such that the meson state not decaying to f is orthogonal to the meson state not decaying to f? In this Letter we propose an alternative T-Violation asymmetry at meson factories which allows its opening to any pair of decay channels. Instead of searching which is the pair of decay channels associated to the T-reverse meson transition, we build an asymmetry which tags the initial states of both the Reference and the T-reverse meson transitions. This observable filters the appropriate final states by means of two measurable survival probabilities. We discuss the methodology to be followed in the analysis of the new observable and the results expected in specific examples.
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Sanjuan, R., Nebot, M., Peris, J. B., & Alcami, J. (2013). Immune Activation Promotes Evolutionary Conservation of T-Cell Epitopes in HIV-1. PLoS. Biol., 11(4), e1001523–10pp.
Abstract: The immune system should constitute a strong selective pressure promoting viral genetic diversity and evolution. However, HIV shows lower sequence variability at T-cell epitopes than elsewhere in the genome, in contrast with other human RNA viruses. Here, we propose that epitope conservation is a consequence of the particular interactions established between HIV and the immune system. On one hand, epitope recognition triggers an anti-HIV response mediated by cytotoxic T-lymphocytes (CTLs), but on the other hand, activation of CD4(+) helper T lymphocytes (T-H cells) promotes HIV replication. Mathematical modeling of these opposite selective forces revealed that selection at the intrapatient level can promote either T-cell epitope conservation or escape. We predict greater conservation for epitopes contributing significantly to total immune activation levels (immunodominance), and when T-H cell infection is concomitant to epitope recognition (transinfection). We suggest that HIV-driven immune activation in the lymph nodes during the chronic stage of the disease may offer a favorable scenario for epitope conservation. Our results also support the view that some pathogens draw benefits from the immune response and suggest that vaccination strategies based on conserved T-H epitopes may be counterproductive.
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